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Increased serum N ‐terminal pro‐B‐type natriuretic peptide and left ventricle diastolic dysfunction in patients with hepatitis C virus infection
Author(s) -
Che W.,
Liu W.,
Wei Y.,
Xu Y.,
Hou L.,
Matsumori A.,
Hu D.
Publication year - 2012
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1111/j.1365-2893.2011.01551.x
Subject(s) - medicine , ventricle , subclinical infection , natriuretic peptide , cardiology , diastole , hepatitis c virus , heart failure , virus , blood pressure , immunology
Summary. Prior studies demonstrated that patients with hepatitis C virus (HCV) infection had higher plasma N ‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP) levels, which may indicate the presence of a subclinical cardiac dysfunction. However, there are few data regarding the echocardiographic assessment in HCV‐infected patients. The objectives of this study were to investigate changes in the left ventricle (LV) with echocardiography and to identify echocardiographic correlates of serum NT‐proBNP levels in HCV‐infected patients. Ninety HCV‐infected patients and 90 age and gender‐matched healthy controls were included. The level of serum NT‐proBNP was higher in the patient group ( P < 0.001). The proportion of patients whose serum NT‐proBNP levels were higher than 125 pg/mL was greater than that of controls (15.56% vs 3.33%, P = 0.011). Echocardiography did not show any significant difference of cardiac structural abnormalities between groups. In the patient group, E, E′ and E/A were lower, and E/E′ was higher. The proportion of patients (13, 14.44%) with impaired diastolic filling (E/A ≤ 0.75; 0.75 < E/A < 1.5 and E/E′ ≥ 10) was greater than that of the control group (3, 3.33%; P = 0.018). Simple regression analysis demonstrated a statistically significant linear correlation between NT‐proBNP levels and left ventricular diastolic diameter (LVDd) ( r = 0.178, P = 0.013), left ventricular posterior wall diastolic thickness (LVPWd) ( r = 0.147, P = 0.023) and mitral E/E’ ( r = 0.414, P = 0.027). Independent correlates of NT‐proBNP levels ( R 2 = 0.34) were older age (β′ = 0.034, P = 0.011) and E/E’ ratio (β′ = 0.026, P = 0.018). In conclusion, the combined analysis of NT‐proBNP and echocardiography showed a possible subclinical left ventricular diastolic dysfunction as evidence of a pathogenic link between HCV and CVD.